2. Academic Validation
  3. The LncRNA RMST-miR-4295-ITPR1 axis: a key mechanism in regulating autophagy in triple-negative breast cancer cells

The LncRNA RMST-miR-4295-ITPR1 axis: a key mechanism in regulating autophagy in triple-negative breast cancer cells

  • BMC Cancer. 2025 Apr 26;25(1):782. doi: 10.1186/s12885-025-14189-7.
Linlei Zhang 1,  Sainan Li 2,  Jiajie Shi 2,  Hao Guo 1,  Bo Wang 1,  Cuizhi Geng 3 4
Affiliations

Affiliations

  • 1 Department of General Surgery, The Second Hospital of Hebei Medical University, Shijiazhuang, Hebei, 050061, China.
  • 2 Department of Breast Center, The Fourth Hospital of Hebei Medical University, No. 169 Tianshan Street, Shijiazhuang, Hebei Province, 050011, China.
  • 3 Department of Breast Center, The Fourth Hospital of Hebei Medical University, No. 169 Tianshan Street, Shijiazhuang, Hebei Province, 050011, China. 46300349@hebmu.edu.cn.
  • 4 Key Laboratory in Hebei Province for Molecular Medicine of Breast Cancer, Shijiazhuang, Hebei, 050011, China. 46300349@hebmu.edu.cn.
PMID: 40287640 DOI: 10.1186/s12885-025-14189-7
Abstract

Background: Triple-negative breast Cancer (TNBC) is an aggressive subtype of breast Cancer with poor prognosis and limited treatment options. Autophagy targeting plays a complex role in tumor resistance. The role of long noncoding RNA (LncRNA) RMST in TNBC progression and its potential involvement in Autophagy regulation remain largely unexplored.

Methods: We performed a bioinformatics analysis using transcriptome Sequencing data to identify differentially expressed genes related to Autophagy and the LncRNA-miRNA-mRNA axis in TNBC. The effects of the LncRNA RMST-miR-4295-ITPR1 axis on TNBC cell proliferation and migration were investigated using CCK-8, EdU, Transwell, and wound healing assays. Additionally, a series of in vitro experiments, including flow cytometry, transmission electron microscopy, and western blotting, were performed to evaluate the role of the LncRNA RMST-miR-4295-ITPR1 axis in regulating Autophagy.

Results: LncRNA RMST competes with ITPR1 mRNA for miR-4295 binding, thereby relieving the miR-4295-mediated suppression of ITPR1 and increasing ITPR1 expression. Overexpression of LncRNA RMST or ITPR1 significantly inhibited TNBC cell proliferation and migration, promoted Apoptosis, and enhanced Autophagy. Conversely, miR-4295 overexpression reversed these effects, confirming the regulatory role of the LncRNA RMST-miR-4295-ITPR1 axis in Autophagy in TNBC.

Conclusions: Our findings indicate that the LncRNA RMST-miR-4295-ITPR1 axis plays a crucial role in regulating Autophagy in TNBC cells. The modulation of this axis may represent a novel therapeutic strategy for inhibiting TNBC progression and overcoming chemoresistance.

Keywords

Autophagy; ITPR1; LncRNA RMST; MiR-4295; TNBC.

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